AUSTIN, Texas—A biologist at The University of Texas at Austin has presented a new theory that sheds light on how organisms, including viruses like HIV, rapidly evolve in the face of vaccines and antibiotics.
Dr. Lauren Ancel Meyers says the new model could help identify genes that increase a pathogen’s ability to evolve quickly against immune responses. Knowing those genes could help scientists develop new and better vaccines.
Meyers’ model predicts that populations can evolve “genetic potential”—genes that can create new traits quickly and simply in changing environments.
“In fluctuating environments, you may get populations evolving right to the brink of evolution,” says Meyers. The organisms are poised to evolve in the face of environmental shifts, because they have genes that can produce a new trait essential to their survival with one or two simple mutations.
Meyers’ model for rapid evolution appears in the Aug. 26 issue of the journal PLoS Computational Biology.
Genetic mutations create the variation that natural selection acts upon. But mutations can be disadvantageous or even deadly, so organisms have evolved so that most simple mutations have little or no biological impact. Mutations are buffered by repair mechanisms and redundancies, like other genes that perform the same function.
For organisms constantly facing new challenges in ever-changing environments, however, there’s an advantage to creating new traits quickly. Previous explanations of rapid evolution have focused on the rate at which mutations occur in the genome. These theories suggest that populations can evolve new traits faster if they are hypermutable, that is, they have faster rates of mutation.
Meyers’ idea is significantly different, because it shows populations can adapt quickly without a faster rate of genetic mutation. Instead, the populations evolve genes that can be easily altered to create new traits.
“Evolution can accelerate without changing the mutation rate itself—it’s the evolution of the ability to evolve—that’s the novel insight of this work,” says Meyers.
Meyers is an assistant professor in the Section of Integrative Biology with a faculty position at the Santa Fe Institute. Co-authors on the paper include Meyers’ father, Dr. Fredric Ancel, from the University of Wisconsin-Milwaukee, and Dr. Michael Lachmann, of the Max Planck Institute in Leipzig, Germany.
For more information contact: Lee Clippard, College of Natural Sciences, 512-232-0675.